HYPOTHESIS: That acetaldehyde induces mitochondrial lipid peroxidations which compromise respiration and oxidative phosphorylation and are responsible for pathology of alcoholism. AIMS - Ia: Ascertain in in vitro experiments that acetaldehyde effects mitochondrial lipid peroxidation in rat liver/heart & ovine heart; 1b: establish MECHANISMS Of peroxidations; IIal: determine in acute in vivo experiments in rates if intraperitoneal injections of acetaldehyde and/or ethanol, in the presence and absence of disulfiram, will cause liver/heart mitochondrial peroxidations; IIa2: determine in chronic in vivo experiments in rats on liquid isocaloric diets plus or minus ethanol and plus or minus presence of disulfiram if ethanol wll induce liver/heart mitochondrial peroxidations; IIB: attempt, in chronic in vivo experiments in rats, to enhance or attenuate respectively mitochondrial peroxidative damage by restricting Vit. Eor supplementing idets with Vits. E & C. SCIENTIFIC BACKGROUND: Acetaldehyde appears to be toxic principle associated with chronic ethanol ingestion with compromises mitochondrial functions. Mitochondria transfer electrons in part to 02 to form 02 minus which forms HOOH which reacts with aldehydes to form 1-dydroxyalkylhydroperoxides wihich react with nucleophiles to: 1) emite light, the intensity of which is enhanced by fluorescers and suppressed by 02, 2) reduce redox dyes 34) sensitize 102 minus formation which, 4) effects lipid peroxidations which may compromise mitochondrial functions. We discoverd acetaldehyde added to mitochondria in metabolic states known to form HOOH elicits chemiluminescence which reflects metabolic state and which responds to ite blickers, uncouplers, ADP, ATP, Vit. C and 02. METHODS: Isolate and identify mitochondrial peroxides by solvent extraction, TLC, HPLC and column chromatography; ethanol/acetaldehyde by HPLC; GC; disulfiram by chelation-spectroscopy; chemiluminescence by scintillation spectroscopy; peroxides assayed enzymatically, iodometrically, iron thiocyante, this barbituric acid, diene conjugation, NBT-reduction, chemiluminescence, horse-radish scopoletin-fluorometric assay; 02 minus polarographically; electronic excitation states: characterized by energy resonance transfer, 02 minus polarographically; electronic excitation states: characterized by energy resonance transfer, 02-sensitization, specific traps (102), kinetics, quenchers, p02, lipid peroxidations. SIGNIFICANCE: Clarify MECHANISMS of acetaldehyde induced mitochondrial toxicities responsible, in part, for pathology of alcoholism.